How do I know if I need medication, or whether therapy alone is enough?

Severity drives the answer. RANZCP guidelines recommend psychotherapy first for mild depression — CBT, IPT, behavioural activation — without an antidepressant. For moderate depression the evidence supports combined treatment: psychotherapy plus a Selective Serotonin Reuptake Inhibitor. For severe depression, medication is started early alongside therapy because waiting for therapy alone to take effect is too slow when functioning has collapsed. Your GP will use PHQ-9 (a nine-question score) and clinical judgement about how much daily life is affected. Other factors that shift toward earlier medication: previous good response, family history of depression that responded to medication, severe sleep or appetite disturbance, suicidal thoughts, or symptoms that have already persisted six-to-eight weeks despite therapy and lifestyle work.

Will antidepressants change who I am?

This is one of the most common — and reasonable — questions in the consulting room. The honest answer from the trial evidence and clinical experience: when antidepressants work, most people describe feeling more like themselves, not less. The flat, numb, withdrawn version isn't usually the baseline — it's the depression. That said, side effects are real. Some people experience emotional blunting at higher doses, where positive emotions feel muted alongside the depressive ones; this is a recognised effect and usually a reason to dose-adjust or switch agents. Sexual dysfunction affects roughly a third of users and warrants discussion rather than silent endurance. Antidepressants are not addictive in the substance-use sense but stopping abruptly can produce a discontinuation syndrome — they should be tapered. If a medication doesn't feel right, that is information your GP wants, not a verdict on you.

My GP wants to order blood tests before treating depression — why, if depression is a mental illness?

Because several physical conditions produce identical symptoms. An underactive thyroid, vitamin B12 deficiency, low iron, vitamin D deficiency, and untreated obstructive sleep apnoea can all mimic or worsen depression — and missing them means treating the wrong problem. RACGP-aligned workup typically includes thyroid function (TSH), full blood count, iron studies, B12 and folate, vitamin D, fasting glucose or HbA1c, and selectively calcium and electrolytes. None of these rule depression in or out — depression remains a clinical diagnosis — but normal results don't dismiss what you're experiencing, and abnormal results may explain part of the picture. Being told 'your bloods are normal so you're fine' is one of the most common dismissive experiences patients describe, and it's not what good practice looks like.

How long until an antidepressant actually works, and how long do I stay on it?

Side effects start in the first week — usually mild nausea, headache, sleep disturbance, sometimes a brief increase in anxiety — and generally settle by week two. Mood improvement typically begins around week two-to-four, with full response by week six-to-twelve. If after six weeks at an adequate dose there has been no meaningful improvement, your GP will reassess: adherence, dose, alternative diagnosis, or a switch. Duration after remission is the part most often shortened too soon. The standard recommendation is to continue at the effective dose for at least six-to-twelve months after you feel well, two years if this is a recurrent depression, and longer if you've had three or more episodes. Stopping early is the single most common reason depression returns.

What is a Mental Health Treatment Plan and how do I get the 10 subsidised psychology sessions?

The Better Access initiative provides Medicare rebates for up to 10 individual psychology sessions per calendar year for eligible mental health conditions, including depression. The pathway: your GP completes a Mental Health Treatment Plan in a longer appointment (MBS items 2700, 2701, 2715 or 2717 depending on consult length and GP training), identifies the goals and refers you to a psychologist, clinical psychologist, accredited mental health social worker, or mental health occupational therapist. The first six sessions are followed by a GP review, then up to four more if clinically indicated. The Medicare rebate covers part of the fee; many psychologists charge a gap, and some bulk-bill. If cost is a barrier, ask about bulk-billing practices, university psychology clinics, headspace centres (under-25s), or free online programs like MindSpot, This Way Up, and MoodGYM that deliver primary-tier CBT without a referral.

What does an integrative GP add to the mainstream depression approach?

The conventional pillars — psychotherapy, medication when indicated, suicide-risk safety planning — are non-negotiable and not where integrative practice differs. Where it adds value is in systematic attention to the modifiable inputs that mainstream care often mentions briefly and moves past: structured exercise prescription (the Cochrane evidence shows an effect size comparable to medication in mild-to-moderate disease), the Mediterranean dietary pattern studied in the SMILES trial, sleep architecture and circadian alignment, alcohol intake, vitamin D and B12 replacement where deficient, omega-3 EPA-predominant supplementation, and screening for the inflammatory and metabolic comorbidities that worsen depression outcomes. It also means engaging seriously with patient preferences around medication, and being transparent about the emerging — and tightly regulated — evidence for newer interventions like rTMS, esketamine, and psychedelic-assisted therapy.

Major depressive disorder

Depression: psychotherapy, medication, and what your bloods can't tell you

By Dr HB Lo, FACRRM Reviewed 18 May 2026 16 min read

Major depressive disorder is a common, treatable illness. Around 1 in 6 Australians experience it.

Diagnosis is clinical: persistent low mood or loss of interest, plus changes to sleep, appetite, energy, concentration, or self-worth, lasting at least two weeks. PHQ-9 grades severity (10+ moderate, 15+ moderately severe, 20+ severe).

First-line for mild-to-moderate is psychotherapy via a Mental Health Treatment Plan; moderate-to-severe usually adds an SSRI (sertraline or escitalopram). Exercise, sleep, alcohol moderation, and Mediterranean-pattern eating each carry independent benefit.

Thoughts of suicide: call Lifeline 13 11 14 or attend your nearest ED.

What depression actually is — and what your bloods can’t tell you

A common experience: you’ve felt flat, exhausted, and uninterested in life for months. You’ve finally gone to your general practitioner. They’ve ordered bloods. The bloods come back, and you’re told they’re normal. “So you’re fine.”

You are not fine. And good clinical practice does not stop there.

Major depressive disorder is a clinical diagnosis — not a blood result. The RANZCP 2020 Mood Disorders Clinical Practice Guideline defines a major depressive episode as five or more of the following symptoms across at least a two-week period, including at least one of either depressed mood or loss of interest and pleasure (anhedonia): persistent low mood, anhedonia, significant appetite or weight change, sleep disturbance, psychomotor change, fatigue, worthlessness or excessive guilt, impaired concentration, and recurrent thoughts of death. The symptoms must cause significant distress or impairment and not be better explained by a substance, medication, or another medical condition.

Around 10% of Australian adults experience MDD in any 12-month period; lifetime prevalence sits around 15–16%, with women affected roughly twice as often as men. Approximately 3,200 Australians die by suicide each year, three-quarters of them male. The condition is common, the treatment evidence is strong, and the AU primary-care pathway is well-defined — but the experience of being dismissed in a brief consultation because a blood panel is “normal” is itself one of the reasons people delay seeking help.

The screening tool the rest of this article will keep referring to is PHQ-9 — a nine-item questionnaire scored 0–27. Thresholds: 5–9 mild, 10–14 moderate, 15–19 moderately severe, 20+ severe. It is not a diagnostic test but a quantification of what you’re already describing, and it lets your GP track change over time rather than guessing.

A. Core clinical — the AU primary-care framework

A first depression assessment in Australian general practice, aligned with RACGP mental health resources and eTG Psychotropic, covers several domains in sequence.

Structured symptom assessment. PHQ-9 for depression severity; the K10 (Kessler Psychological Distress Scale) is widely used in AU general practice, with scores ≥22 indicating high distress. The DASS-21 separates depression, anxiety, and stress components.

Bipolar screen — non-negotiable. Before any antidepressant is prescribed, your GP needs to ask about past episodes of elevated mood, decreased need for sleep, racing thoughts, grandiosity, or risk-taking behaviour. The reason is clinical safety: starting a Selective Serotonin Reuptake Inhibitor in someone with undiagnosed bipolar disorder can precipitate a manic switch. The Mood Disorder Questionnaire (MDQ) is a brief tool used for this. If bipolarity is suspected, the referral is to psychiatry for mood stabiliser consideration (RANZCP 2020) — lithium, valproate, lamotrigine, or atypical antipsychotic.

Suicidality assessment. A structured conversation, not a checkbox. Current ideation (passive thoughts of being better off dead vs active thoughts of ending one’s life), plan, intent, preparation, access to means, prior attempts, family history of suicide, and protective factors. This is the most important part of the consultation in moderate-to-severe presentations. Safety planning, crisis-line information, and clear escalation pathways are documented before you leave.

Organic mimics — the bloods that matter. Several physical conditions produce or worsen depressive symptoms and need to be excluded or treated:

Thyroid function (TSH) — hypothyroidism is a classic mimic, particularly in women.
Full blood count and iron studies (ferritin, transferrin saturation) — iron-deficiency anaemia and anaemia of chronic disease both contribute to fatigue and low mood.
Vitamin B12 and folate — deficiency is more common in vegans, the elderly, long-term metformin users, and those with malabsorption.
Vitamin D — deficiency carries modest mood effects, especially with seasonal pattern.
HbA1c or fasting glucose — undiagnosed diabetes and metabolic syndrome correlate with depression risk.
Calcium and electrolytes — selectively, especially in older patients.
Sleep study — if obstructive sleep apnoea is suspected (snoring, witnessed apnoeas, daytime sleepiness, BMI ≥30).

Substance use screen. Alcohol intake (often used as self-medication and itself depressogenic), cannabis, methamphetamine, opioids, and benzodiazepines all interact with mood. NPS MedicineWise provides AUDIT-C and ASSIST screening tools used in general practice.

Trauma history and adverse childhood experiences (ACEs). Childhood abuse, neglect, intimate partner violence, and adult trauma significantly increase lifetime depression risk and inform treatment choice — trauma-focused therapies (TF-CBT, EMDR) may be preferred when trauma is central.

Perinatal screen. The Edinburgh Postnatal Depression Scale (EPDS) is the AU general-practice standard for antenatal and postnatal mood screening, typically administered at the 6-week postnatal check.

Mental state examination. Appearance, behaviour, speech, mood and affect, thought form and content, perception, cognition, insight. In older patients depression can mimic dementia (“pseudodementia”) — cognitive screening (MMSE, MoCA) with treatment trial often clarifies.

B. Evidence appraisal — treatment options ranked by evidence

Psychotherapy — first-line for mild-to-moderate

The RANZCP 2020 guideline is explicit: psychological therapy is first-line for mild depression, with antidepressants not routinely recommended. The reasoning is supported by Fournier’s 2010 JAMA meta-analysis, which found that antidepressant effect over placebo is minimal in mild depression and increases progressively with severity.

The trial-tested therapies for depression:

Cognitive behavioural therapy (CBT) — the most extensively studied; targets the maintenance loop between thoughts, emotions, behaviour, and physiology.
Interpersonal therapy (IPT) — focuses on grief, role transitions, role disputes, and interpersonal deficits.
Behavioural activation — structured re-engagement with rewarding activities; effective as a standalone intervention.
Mindfulness-based cognitive therapy (MBCT) — strong evidence for relapse prevention in recurrent depression.
Acceptance and commitment therapy (ACT) — values-based behavioural engagement.

Network meta-analyses, including the work of Cuijpers and colleagues, show comparable efficacy across these modalities for most patients, with the choice often driven by therapist availability and patient preference.

Antidepressants — when severity warrants it

For moderate-to-severe depression, Cuijpers’ 2014 JAMA Psychiatry analysis shows combined psychotherapy plus antidepressant treatment is superior to either alone. Cipriani’s 2018 Lancet network meta-analysis of 522 trials and ~116,000 patients confirmed that all 21 antidepressants studied were more effective than placebo, with sertraline and escitalopram emerging as having the best combination of efficacy and tolerability.

First-line in AU practice (per eTG Psychotropic and Australian Medicines Handbook):

Sertraline — start 50 mg daily, range 50–200 mg. Often the first choice; minimal cytochrome P450 interactions; favourable safety profile in pregnancy and breastfeeding.
Escitalopram — start 10 mg daily, range 10–20 mg. QT prolongation at doses above 20 mg.

Other PBS-listed first- and second-line agents:

Citalopram 20–40 mg (QT-prolonging at higher doses; maximum 20 mg in over-65s).
Fluoxetine 20–80 mg — long half-life; useful where adherence is variable; most extensive pregnancy data.
Paroxetine 20–60 mg — significant discontinuation syndrome; avoid in elderly and in first-trimester pregnancy.
Venlafaxine (SNRI) 75–225 mg — useful for SSRI non-responders and where pain is comorbid; BP monitoring at higher doses.
Desvenlafaxine 50–100 mg — venlafaxine’s active metabolite; fewer interactions.
Duloxetine (SNRI) 30–120 mg — PBS Authority Required; particularly useful when comorbid neuropathic pain.
Mirtazapine 15–45 mg at night — sedating, appetite-stimulating; useful when insomnia and poor appetite dominate; less sexual dysfunction.
Vortioxetine 5–20 mg — PBS-listed; modest cognitive benefit signal; nausea is the main early side effect.
Agomelatine 25–50 mg at night — melatonergic; requires liver function monitoring.

Weeks to effect and side-effect counselling:

First 1–2 weeks — nausea, headache, sleep disturbance, sometimes a brief increase in anxiety. These usually settle. Suicidality monitoring is critical in this window, particularly in those under 25 — the FDA-warned phenomenon of treatment-emergent suicidality is real but the absolute risk increase is small, and untreated depression carries higher suicide risk overall.
Weeks 2–4 — initial mood response. PHQ-9 reduction of 50% or more is considered a response.
Weeks 6–12 — full response and remission (PHQ-9 below 5).
Sexual dysfunction — affects roughly 30–50% of SSRI/SNRI users. Decreased libido, delayed orgasm, erectile dysfunction. Switching to mirtazapine, vortioxetine, or bupropion (smoking-cessation PBS only in Australia) is reasonable when persistent.
Discontinuation syndrome — flu-like symptoms, dizziness, electric-shock sensations, mood disturbance on abrupt cessation. Most marked with paroxetine, venlafaxine, and desvenlafaxine. Tapering over 4–8 weeks (longer for some) is standard; fluoxetine self-tapers because of its long half-life.

STAR*D — context and limitations

The STAR*D trial — Sequenced Treatment Alternatives to Relieve Depression, US, ~4,000 patients — remains the largest naturalistic study of stepped antidepressant treatment. Cumulative remission after four sequential treatment steps reached around 67%. The trial drives current understanding that switching agents and augmentation strategies are reasonable next steps after initial non-response, but later re-analyses have highlighted methodological limitations and that the cumulative remission figure includes patients who later relapsed. Clinically, STAR*D supports the principle of sequential trials rather than premature labelling of treatment-resistance.

Treatment-resistant depression

The working definition: failure of two adequate antidepressant trials at therapeutic dose for 6–8 weeks each. At this point RANZCP recommends psychiatric referral for consideration of:

Augmentation — lithium (with therapeutic drug monitoring), atypical antipsychotic (quetiapine, aripiprazole — PBS Authority Required for treatment-resistant depression), or triiodothyronine (T3).
Class switch — SSRI to SNRI to mirtazapine to a TCA or MAOI under specialist care.
Electroconvulsive therapy (ECT) — the most effective treatment for severe, psychotic, catatonic, or rapidly deteriorating depression; modern anaesthesia and unilateral techniques have substantially reduced cognitive side effects compared with older bilateral ECT.
Repetitive transcranial magnetic stimulation (rTMS) — PBS-listed since 2021 for treatment-resistant depression meeting specific criteria (≥2 antidepressant trials failed); typically 4–6 weeks of daily outpatient sessions (MBS items 14224–14227 range).
Intranasal esketamine (Spravato) — TGA-approved for treatment-resistant depression; specialist-administered in supervised settings; not PBS-subsidised, so private cost is substantial (around $400–500 per dose, with multiple doses required).

HRSD vs PHQ-9

Trials typically use the Hamilton Rating Scale for Depression (HRSD or HAM-D), administered by a clinician. PHQ-9 is patient-reported. The scales correlate well enough for clinical use, but they are not interchangeable in trial interpretation — a “50% HRSD reduction” in a trial is the response standard most antidepressant evidence is built on.

C. AU access pathways — Better Access, MHTP, bulk-billing reality

(MBS / PBS items verified 2026-05-18 via WebSearch — workspace egress to mbsonline.gov.au and pbs.gov.au remains blocked; spot-checks confirm current.)

The Better Access initiative is the main mechanism through which Australians access Medicare-rebated psychological therapy for depression.

The pathway:

Book a longer appointment with your GP for a Mental Health Treatment Plan (MHTP). MBS items used are 2700, 2701, 2715, or 2717, depending on consult length and whether your GP holds Mental Health Skills Training.
The MHTP documents diagnosis, goals, and chosen provider type, and generates a referral.
You attend up to 6 individual psychology sessions, then return to the GP for a review (MBS 2712).
After review, up to 4 further sessions are available if clinically indicated — total 10 individual sessions per calendar year (currently; this was temporarily increased to 20 during COVID and reverted in 2023).
Up to 10 group sessions per calendar year are separately available.

Provider types: clinical psychologists (higher rebate), registered psychologists, accredited mental health social workers, accredited mental health occupational therapists.

The cost-gap reality. Medicare rebates cover only part of the session fee. A clinical psychologist’s standard fee is often $250–$280; the Medicare rebate is around $141 for a clinical psychologist and around $96 for a general psychologist, leaving a gap of $100+ per session common in metropolitan areas. Bulk-billing psychology practices exist but are increasingly difficult to access, with waiting lists commonly 2–6 months in metropolitan areas and longer in rural and regional Australia.

Workarounds when cost or wait time is the barrier:

headspace — free or low-cost mental health support for those aged 12–25, including online and in-centre options.
Beyond Blue — telephone and webchat support, 1300 22 4636.
This Way Up — AU-developed online CBT programs aligned with primary-tier guidelines; clinician-supervised version is low-cost.
MindSpot Clinic — free, telephone-and-online clinician-supported CBT for adults.
MoodGYM — free interactive CBT modules.
University psychology clinics — provisional psychologists supervised by senior staff; substantially reduced fees.
Community mental health teams — state-based, free, but generally reserved for moderate-to-severe presentations or those with complex needs.
Aboriginal Medical Services and Aboriginal Mental Health Worker programs — culturally safe options for ATSI patients.

The waitlist and gap-fee reality is structural, not invented — and naming it explicitly is part of honest pathway planning rather than promising access that doesn’t exist in the postcode you’re in.

D. Lifestyle and adjunctive evidence

The lifestyle pillars are not a substitute for psychotherapy and medication when those are indicated — but the evidence is strong enough that they belong in the prescription, not as an afterthought.

Exercise. The Cochrane 2013 review of exercise for depression — 39 trials, ~2,300 participants — found a moderate effect size, comparable to antidepressants and psychotherapy in mild-to-moderate depression. Larger more-recent network meta-analyses, including Heissel BMJ 2024, reinforce this with dance, walking, jogging, yoga, and strength training all showing benefit. The pragmatic prescription: 150 minutes per week of moderate aerobic activity plus 2 sessions of resistance training, scaled to current capacity. Adherence is the limiting factor in depressed patients — structured programs, accountability, and starting very small all help.

Diet. The SMILES trial (Jacka, BMC Med 2017) randomised 67 adults with moderate-to-severe depression to dietary support (Mediterranean pattern) versus social support and found significant reduction in depression scores in the diet group. The trial is small and the comparator is debated, but the broader observational evidence linking Mediterranean dietary pattern to reduced depression risk is consistent. Practical translation: vegetables, legumes, fruit, whole grains, nuts, olive oil, fish, moderate dairy, limited processed and ultra-processed foods.

Sleep and circadian alignment. Sleep disturbance is bidirectional with depression — improving one improves the other. CBT for insomnia (CBT-I) is first-line for chronic insomnia and reduces depression severity independently. Bright morning light exposure (10–30 minutes outdoors) supports circadian alignment.

Alcohol. Alcohol is depressogenic — it fragments sleep architecture, alters serotonergic and GABAergic neurotransmission, and is frequently used as self-medication that worsens the underlying problem. Reduction to within NHMRC guidelines (no more than 10 standard drinks per week and no more than 4 on any one day) is part of the treatment plan.

Cannabis. Cannabis carries a paradoxical relationship with depression — short-term anxiolysis with longer-term anhedonia, motivational deficit, and psychosis risk especially in younger users. AU evidence for cannabis-based therapies in depression remains weak, and TGA Special Access Scheme pathways exist for specific indications but not first-line for major depression.

Omega-3 fatty acids. EPA-predominant supplementation (1–2 g/day of EPA, ratio EPA:DHA > 2:1) shows modest mood benefit in meta-analyses, particularly as an adjunct rather than monotherapy.

Vitamin D. Replacement where deficient (25-hydroxyvitamin D < 50 nmol/L) carries modest mood benefit; routine supplementation in vitamin-D-sufficient individuals does not.

Ketamine and esketamine. Intranasal esketamine (Spravato) is TGA-approved for treatment-resistant depression and administered in supervised clinical settings. Racemic IV ketamine is used off-label in specialist clinics and ketamine-assisted psychotherapy programs. Neither is PBS-subsidised; private costs are substantial. The AU “ketamine clinic” landscape varies in regulatory rigour — TGA-approved protocols and credentialled psychiatrist oversight are markers of quality.

Psychedelic-assisted psychotherapy. Since July 2023, the TGA has permitted MDMA for treatment-resistant PTSD and psilocybin for treatment-resistant depression under the Authorised Prescriber pathway — meaning a psychiatrist must apply for individual authorisation, and treatment is delivered in tightly regulated contexts with substantial associated psychotherapy. Access in practice remains extremely limited, costs are several thousand dollars per course, and the AU regulatory model is more restrictive than the marketing of overseas retreats and online programs suggests. Claims that psilocybin or MDMA can be self-administered or accessed casually for depression are inconsistent with TGA scheduling and the Authorised Prescriber model.

E. Special populations

Perinatal. Pregnancy and the first 12 months postpartum carry distinctive risks. EPDS is the standard screen, used antenatally and at 6 weeks postpartum. Sertraline is the preferred SSRI in breastfeeding (low transfer into breastmilk and extensive safety data); escitalopram and citalopram are also reasonable. Paroxetine has a small first-trimester cardiac defect signal in some — but not all — data and is generally avoided. Postpartum psychosis is a psychiatric emergency requiring mother-and-baby unit admission. Beyond Blue’s perinatal program and PANDA are AU consumer resources.

Aboriginal and Torres Strait Islander Australians. Higher psychological distress and suicide rates than the non-Indigenous population, reflecting intergenerational trauma, social determinants, and access barriers. Culturally safe pathways include Aboriginal Medical Services, 13YARN (13 92 76 — Aboriginal and Torres Strait Islander crisis support), Social and Emotional Wellbeing programs, and Aboriginal Mental Health Workers. The MBS ATSI Health Assessment (item 715) includes mental health screening.

Older adults. Start low, go slow. SSRIs are preferred; lower starting doses; sodium monitoring at 1–2 weeks (SIADH and hyponatraemia risk); avoid tricyclic antidepressants (anticholinergic, fall risk) and paroxetine. Fall risk is increased with all serotonergic antidepressants and warrants discussion. The Geriatric Depression Scale (GDS) is the validated tool in this population. Pseudodementia — depression mimicking cognitive decline — is common and an antidepressant trial can clarify.

Adolescents. Fluoxetine is the only SSRI with strong evidence (and TGA/FDA approval) in adolescents; other SSRIs are second-line. The FDA black-box warning about treatment-emergent suicidality in under-25s reflects real but small absolute risk — close monitoring in the first 2–4 weeks is essential, but untreated adolescent depression carries its own suicide risk that is generally higher. headspace and Black Dog Institute youth pathways are AU specialty consumer resources. School counselling, family involvement, and screen-time and substance-use discussions belong in the plan.

Chronic pain comorbid. Depression and chronic pain frequently coexist and amplify each other. Duloxetine carries PBS approval for chronic pain syndromes and is often a logical choice when both are present. Tricyclic antidepressants at low dose remain useful for neuropathic pain and migraine prophylaxis but generally not for depression itself.

Postnatal depression. Up to one in seven Australian mothers experience postnatal depression. The pathway through PANDA, Maternal and Child Health Nurses, and GP MHTP is well-developed but underused. Asking new fathers about mood is part of best practice — paternal postnatal depression is real, underdiagnosed, and treatable.

When to escalate / urgent referral

Same-day or emergency department escalation:

Active suicidal ideation with plan, intent, or preparation
A recent suicide attempt
Psychotic features (delusions or hallucinations) in the context of depression
Severe weight loss, self-neglect, or catatonia
Postpartum psychosis
Severe agitation or inability to engage with outpatient care

Routine psychiatric referral:

Failure of two adequate antidepressant trials (treatment-resistant depression)
Suspected bipolar disorder
Complex comorbidity — eating disorder, personality disorder, severe substance use disorder
Perinatal depression with severity or risk concerns
Severe adolescent depression
Consideration of ECT, rTMS, or esketamine

What this article is and is not

This is general health information drawn from current Australian primary-care guidelines — RANZCP 2020 Mood Disorders, RACGP mental health resources, Therapeutic Guidelines, AMH, NPS MedicineWise, Beyond Blue, and Black Dog Institute — and major depression trials including STAR*D, the Cipriani 2018 Lancet network meta-analysis, the Cuijpers 2014 combined-treatment analysis, the SMILES dietary trial, and Cochrane reviews on exercise. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about specific treatment — including whether to start, change, or stop medication — are made with your own general practitioner and treating clinicians, who can take your full history into account.

Depression is treatable. Not always quickly, not always with the first agent, and rarely with a single intervention alone — but the response rates are high, and ongoing remission for most is realistic. Being dismissed in a brief consultation is not the standard of care, and finding a GP who will sit with the complexity is part of getting better.

For Australian consumer-friendly sources: Beyond Blue, Black Dog Institute, HealthDirect — Depression, Better Health Channel, Head to Health, SANE Australia.

For acute mental-health crisis: Lifeline 13 11 14, Beyond Blue 1300 22 4636, 13YARN 13 92 76, Suicide Call Back Service 1300 659 467.

Sources cited

Frequently asked questions

How do I know if I need medication, or whether therapy alone is enough?

Severity drives the answer. RANZCP guidelines recommend psychotherapy first for mild depression — CBT, IPT, behavioural activation — without an antidepressant. For moderate depression the evidence supports combined treatment: psychotherapy plus a Selective Serotonin Reuptake Inhibitor. For severe depression, medication is started early alongside therapy because waiting for therapy alone to take effect is too slow when functioning has collapsed. Your GP will use PHQ-9 (a nine-question score) and clinical judgement about how much daily life is affected. Other factors that shift toward earlier medication: previous good response, family history of depression that responded to medication, severe sleep or appetite disturbance, suicidal thoughts, or symptoms that have already persisted six-to-eight weeks despite therapy and lifestyle work.
Will antidepressants change who I am?

This is one of the most common — and reasonable — questions in the consulting room. The honest answer from the trial evidence and clinical experience: when antidepressants work, most people describe feeling more like themselves, not less. The flat, numb, withdrawn version isn't usually the baseline — it's the depression. That said, side effects are real. Some people experience emotional blunting at higher doses, where positive emotions feel muted alongside the depressive ones; this is a recognised effect and usually a reason to dose-adjust or switch agents. Sexual dysfunction affects roughly a third of users and warrants discussion rather than silent endurance. Antidepressants are not addictive in the substance-use sense but stopping abruptly can produce a discontinuation syndrome — they should be tapered. If a medication doesn't feel right, that is information your GP wants, not a verdict on you.
My GP wants to order blood tests before treating depression — why, if depression is a mental illness?

Because several physical conditions produce identical symptoms. An underactive thyroid, vitamin B12 deficiency, low iron, vitamin D deficiency, and untreated obstructive sleep apnoea can all mimic or worsen depression — and missing them means treating the wrong problem. RACGP-aligned workup typically includes thyroid function (TSH), full blood count, iron studies, B12 and folate, vitamin D, fasting glucose or HbA1c, and selectively calcium and electrolytes. None of these rule depression in or out — depression remains a clinical diagnosis — but normal results don't dismiss what you're experiencing, and abnormal results may explain part of the picture. Being told 'your bloods are normal so you're fine' is one of the most common dismissive experiences patients describe, and it's not what good practice looks like.
How long until an antidepressant actually works, and how long do I stay on it?

Side effects start in the first week — usually mild nausea, headache, sleep disturbance, sometimes a brief increase in anxiety — and generally settle by week two. Mood improvement typically begins around week two-to-four, with full response by week six-to-twelve. If after six weeks at an adequate dose there has been no meaningful improvement, your GP will reassess: adherence, dose, alternative diagnosis, or a switch. Duration after remission is the part most often shortened too soon. The standard recommendation is to continue at the effective dose for at least six-to-twelve months after you feel well, two years if this is a recurrent depression, and longer if you've had three or more episodes. Stopping early is the single most common reason depression returns.
What is a Mental Health Treatment Plan and how do I get the 10 subsidised psychology sessions?

The Better Access initiative provides Medicare rebates for up to 10 individual psychology sessions per calendar year for eligible mental health conditions, including depression. The pathway: your GP completes a Mental Health Treatment Plan in a longer appointment (MBS items 2700, 2701, 2715 or 2717 depending on consult length and GP training), identifies the goals and refers you to a psychologist, clinical psychologist, accredited mental health social worker, or mental health occupational therapist. The first six sessions are followed by a GP review, then up to four more if clinically indicated. The Medicare rebate covers part of the fee; many psychologists charge a gap, and some bulk-bill. If cost is a barrier, ask about bulk-billing practices, university psychology clinics, headspace centres (under-25s), or free online programs like MindSpot, This Way Up, and MoodGYM that deliver primary-tier CBT without a referral.
What does an integrative GP add to the mainstream depression approach?

The conventional pillars — psychotherapy, medication when indicated, suicide-risk safety planning — are non-negotiable and not where integrative practice differs. Where it adds value is in systematic attention to the modifiable inputs that mainstream care often mentions briefly and moves past: structured exercise prescription (the Cochrane evidence shows an effect size comparable to medication in mild-to-moderate disease), the Mediterranean dietary pattern studied in the SMILES trial, sleep architecture and circadian alignment, alcohol intake, vitamin D and B12 replacement where deficient, omega-3 EPA-predominant supplementation, and screening for the inflammatory and metabolic comorbidities that worsen depression outcomes. It also means engaging seriously with patient preferences around medication, and being transparent about the emerging — and tightly regulated — evidence for newer interventions like rTMS, esketamine, and psychedelic-assisted therapy.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.